Electronic Letters to:
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eLetters: Electronic letters published:
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metabolic syndrome in patients with learning disabilities
- Padmaja Sivakumar (5 July 2007)
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Metabolic disease in community traeted patients-confounders or confirmations?
- Saddichha Sahoo (1 August 2007)
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Metabolic and endocrine disease in patients taking antipsychotic medication
- Oliver D Howes, Shubulade Smith, Stephanie A. Amiel, Fiona P. Gaughran (10 August 2007)
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Metabolic and cardiovascular risk in people treated with antipsychotics: case-control or survey?
- Anindya Banerjee, Debasish Basu (6 September 2007)
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Re: Metabolic and cardiovascular risk in people treated with antipsychotics: case-control or survey?
- Paul Mackin, Peter Gallagher (25 September 2007)
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Padmaja Sivakumar, SHO in psychiatry of learning disbility, Cheshire and wirral partnership NHS trust
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padmajasivakumar{at}hotmail.com Padmaja Sivakumar
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The authors of this study highlight the importance of screening and management of metabolic syndrome in patients with severe mental illness. This is of paramount importance particularly in patients with learning disability as they have high rates of both physical and psychiatric co morbidities compared to general population (Welsh office,1996). In addition to this Considerable evidence points to a disparity between the health of people with learning disability and general population which was also highlightened in the MENCAP reports 'Treat me right' and 'death by indefference'. Suggested causes for this disparity include specific patterns of complex health needs associated with the aetiology of their learning disability, sensory and communication difficulties, reliance on carers to communicate their health needs and also barriers to health care accesability due to poor professional knowledge and attitudes. The Government white paper 'Valuing people' (DOH 2001) acknowledges this disparity and identifies the improved health care of people with learning disability as a key outcome. But the document is a little unclear on how these aims will be acheived. As the authors of this study point out there are few studies specifically examining the impact of different models of care on psysical well being and comorbidities in patients with severe mental illness, which is also the case in patients with learning disability. There is a pressing need for evidence based integrated models of care for delivering highstandards of care for this patient group. References: Department of Health (2001)Valuing people:A new Strategy for Learning Disability for the 21st Century. London:Stationery office. Welsh Office (1996) Welsh Health Survey 1995. Cardiff: Welsh Office. |
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Saddichha Sahoo, Resident in Psychiatry Central Institute of Psychiatry< Ranchi, India
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saddichha{at}gmail.com Saddichha Sahoo
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After going though the findings of Mackin et al (2007) in their study of metabolic disease in patients treated in the community, I find that there are several methodological problems which I believe may limit their findings. Firstly, the recruitment procedure is not very clear. Were the patients invited on a random basis or consecutively? There is also an inherent selection bias as less than half of the initially targeted 198 patients agreed to finally participate. It could be possible that, once explained about the study, only those patients agreed to participate who had clear risk factors. Finally, the presence of poly-pharmacy, especially the use of SSRIs in one third of the sample and mood stabilizers such as Lithium and Valproate in another third, clearly point to a multi- etiological basis. The overwhelming amount of substance use in study sample is another major limiting factor. Also I am unable to understand what prospective study was conducted since neither duration nor the findings have been reported. References: Mackin, P., Bishop, D., Watkinson, H., Gallagher, P., Ferrier, I. N. (2007) Metabolic disease and cardiovascular risk in people treated with antipsychotics in the community. British Journal of Psychiatry, 191, 23 - 29. |
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Oliver D Howes, Clinical lecturer Institute of Psychiatry, Shubulade Smith, Stephanie A. Amiel, Fiona P. Gaughran
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o.howes{at}iop.kcl.ac.uk Oliver D Howes, et al.
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We read the paper by Mackin and colleagues with interest. Although the authors report that previous work has not included insulin or HOMA assessment, their work does in fact build on previous findings of abnormal glucose-insulin homeostasis in patients taking antipsychotic medication (Howes et al, 2004;Henderson et al, 2006). Mackin et al’s work extends previous studies by looking at a representative community sample of patients with a range of mental illnesses. Their finding of elevated markers of metabolic dysfunction and cardiovascular risk is a significant concern, especially given that the elevation was found despite the control group comprising an unspecified proportion of relatives, who, in themselves, may be more likely to have cardiovascular risk factors. The reduction in life-expectancy related to antipsychotic treatment induced obesity alone may entirely offset the therapeutic benefits of the most effective antipsychotic medication, clozapine (Fontaine et al, 2001;Howes et al, 2003). Furthermore evidence indicates that, despite guidelines, United Kingdom psychiatric services provide inadequate assessment and intervention for metabolic and endocrine dysfunction in patients taking antipsychotic medications (Taylor et al, 2004). This suggests that systematic approaches to the assessment and intervention for metabolic and endocrine dysfunction and cardiovascular risk factors need to be implemented. The challenge is to develop approaches that can be maintained in everyday practice. Yours sincerely Dr Oliver D. Howes*, Dr Shubulade Smith*, Professor Stephanie A. Amiel**, Dr Fiona P. Gaughran* *Institute of Psychiatry, King's College London, Camberwell, London, SE5 8AF, UK **Department of Diabetes, New Medical School Building, GKT School of Medicine, King's College, London, UK Reference List 1. Fontaine, K. R., Heo, M., Harrigan, E. P., et al (2001) Estimating the consequences of anti-psychotic induced weight gain on health and mortality rate. Psychiatry Res., 101, 277-288. 2. Henderson, D. C., Copeland, P. M., Borba, C. P., et al (2006) Glucose metabolism in patients with schizophrenia treated with olanzapine or quetiapine: a frequently sampled intravenous glucose tolerance test and minimal model analysis. J.Clin.Psychiatry, 67, 789-797. 3. Howes, O., Ohlsen, R., and Pilowsky, L. S. (2003) Effect of clozapine on mortality. Br.J.Psychiatry, 183, 460. 4. Howes, O. D., Bhatnagar, A., Gaughran, F. P., et al (2004) A prospective study of impairment in glucose control caused by clozapine without changes in insulin resistance. Am.J Psychiatry, 161, 361-363. 5. Taylor, D., Young, C., Essop, R., et al (2004) Testing for diabetes in hospitalised patients prescribed antipsychotic drugs. Br J Psychiatry, 185, 152-156. |
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Anindya Banerjee, Senior Resident Post Graduate Institute of Medical Education and Research, chandigarh, Debasish Basu
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dr.banerjee{at}gmail.com Anindya Banerjee, et al.
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Mackin et al. (2007) have highlighted the significantly higher risk of cardiovascular and metabolic diseases in severe mental illness, compared to a control group. Rates of metabolic syndrome and cardiovascular risk similar to schizophrenia have been reported in bipolar disorders and atypical antipsychotics have been approved for treatment of bipolar disorders (Birkenaes et al., 2007; Fagiolini et al., 2005). This implies that all such populations should be studied for putative long-term adverse outcomes, as has been done in this timely study. Some methodological issues, however, need clarification. According to the authors, the current study is a case control study. By definition, a case-control study starts with an outcome and then traces back in time to investigate exposure to putative risk factors in groups with and without the outcome (Lewallen & Courtright, 1998). It then generates a measure of the relative risk with regard to a given risk factor. In the current study, the authors have started with a group of mentally ill patients on antipsychotics and studied the prevalence of metabolic disease and cardiovascular risk and compared those with a control group. Thus, in our understanding, the study has really used a survey design along with a control group. The use of a control group alone does not justify the label of a ‘case control study’. As an important corollary of this distinction, the sample size is rather low for a community-based survey. The authors mention, as the background for the study, that comparative data for physical comorbidity in people with diagnoses other than schizophrenia are sparse; unfortunately, the study itself fails to generate such data due to the inadequate sample size. We feel that the authors have gone beyond their brief (as stated in Aims of the abstract) to analyze the effect of individual factors such as diagnoses, type of antipsychotics medication and smoking; not surprisingly, they failed to emerge with convincing findings as the sample was underpowered to generate such data. Finally, we wonder if the inclusion of several patients with depression and anxiety is appropriate for a study on ‘severe mental illness’, a term traditionally reserved for psychotic and bipolar disorders. The common denominator of the study population seems to be ‘treated with antipsychotics’ as mentioned in the title, rather than ‘severe mental illness’ as mentioned in the Aims of the abstract. It is interesting to note that the type of antipsychotics had no impact on the outcome measures (except serum insulin). If replicated on a much larger community sample, this so-called ‘negative’ finding could potentially have far-reaching implications regarding choice of treatment. Another important factor in the secondary analysis could have been the duration of treatment with antipsychotics and the dosages used. In a recent study, higher doses of medication were found to be associated with increased cardiovascular risk scores (Osborn et al., 2006). Using the dosage and duration of antipsychotic in the analysis could provide some important insights regarding true impact of antipsychotics on the outcome measures. This study, like several others, reiterates that patients treated with antipsychotics are at heightened risk for cardiovascular events and metabolic syndrome. Longitudinal studies are needed to explore the relative contribution of putative etiological factors towards physical comorbidity in severe mental illness. REFERENCES Birkenaes, A.B., Opjordsmoen, S., Brunborg, C., Engh, J.A., Jonsdottir, H., Ringen, P.A. et al. (2007) The level of cardiovascular risk factors in bipolar disorder equals that of schizophrenia: a comparative study. Journal of Clinical Psychiatry, 68, 917-923. Fagiolini, A., Frank, E., Scott, J.A., Turkin, S., Kupfer, D.J. (2005) Metabolic syndrome in bipolar disorder: findings from the Bipolar Disorder Center for Pennsylvanians. Bipolar Disorders, 7, 424–430. Lewallen, S., Courtright, P. (1998) Epidemiology in Practice: Case- Control Studies. Community Eye Health, 11, 57-58. Mackin, P., Bishop, D., Watkinson, H., Gallagher, P., Ferrier, I.N. (2007) Metabolic disease and cardiovascular risk in people treated with antipsychotics in the community. British Journal of Psychiatry, 191, 23- 29. Osborn, D. P. J., Nazareth, I., King, M. B. (2006) Risk for coronary heart disease in people with severe mental illness: cross-sectional comparative study in primary care. British Journal of Psychiatry, 188, 271 -277. |
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Paul Mackin, Senior Lecturer Newcastle University, Peter Gallagher
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paul.mackin{at}ncl.ac.uk Paul Mackin, et al.
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We thank Dr Banerjee for his interest in our study and for the concerns he raises about some of the methodological aspects of the study. Dr Banerjee is correct to point out that our study is not a case-control design in the purest epidemiological sense, i.e. a study in which patients who have developed a disease are identified and their past exposure to aetiological factors is compared with that of controls or referents who do not have do not have the disease. Our study is conceptually similar to the a case-control design, although we accept that both our own study and case -control studies are inherently vulnerable to methodological weaknesses as discussed in a recent paper in this journal (Lee et al, 2007). We selected individuals who had been ‘exposed’ to a diagnosis of severe mental illness and to antipsychotic treatment in order to ascertain whether or not this population was at an increased risk for cardio-metabolic disease, compared with a control group who had not undergone this exposure (Mackin et al, 2007). We also accept, and indeed acknowledge in our paper, that the sample size is relatively small. However, we found highly statistically significant differences between patients and controls across a number of outcomes. The analysis of effect of diagnosis, type of antipsychotic medication and smoking status was not a primary aim of our study, but was a secondary analysis. It may be the case that increasing the sample size further would have added power to the study to detect differences in these variables. Notwithstanding, emerging evidence from studies in patients with bipolar disorders points to an excess of cardio-metabolic disease in these patients which is comparable to that in schizophrenia, thus suggesting that the similar rates of cardiovascular and metabolic risk across our diagnostic groups is a true finding. Dr Banerjee questions the appropriateness of the term ‘severe mental illness’ in our study. The vast majority (75.6%) of subjects had a diagnosis of schizophrenia, bipolar disorder or schizo-affective disorder. Within the ‘other’ category (comprising 24.4%) many of these patients had suffered from episodes of psychotic depression and other severe depressive disorders requiring antipsychotic treatment. Although the use of the word ‘severe’ may be called into question, we are confident that this is an appropriate descriptor. We await larger, prospective studies designed specifically to tease out the aetiological factors that contribute to an excess of cardio- metabolic risk and ultimately an excess mortality rate in this population. We hope our study has gone some way to highlighting the need for vigilant monitoring and appropriate intervention in this high-risk group of patients. Dr Paul Mackin (paul.mackin@ncl.ac.uk) Mr Peter Gallagher Institute of Neuroscience Newcastle University, UK Lee, W., Bindman, J., Ford, T., et al (2007) Bias in psychiatric case -control studies. British Journal of Psychiatry, 190, 204-209 Mackin, P., Bishop, D., Watkinson, H., et al (2007) Metabolic disease and cardiovascular risk in people treated with antipsychotics in the community. British Journal of Psychiatry, 191, 23-29 Declaration of interest P.M.and P.G have received honoraria for educational meetings from pharmaceutical companies. |
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